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A plant pathogen has a secret weapon
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showed that AsA, rather than its metabolites, was transported. Endogenously produced AsA, monitored following the application of L-galactono-1,4-lactone (GAL-L) (the immediate precursor of AsA) to source leaves, was translocated in the same way. This was shown by a doubling of AsA levels in the shoot tip above the application leaf and no change in the mature leaves below it. GAL-L itself was not transported. Furthermore, because AsA levels in sinks increased in proportion to levels in the application leaf, sink tissue AsA content appears to be directly influenced by availability in source tissues.
TRENDS in Plant Science Vol.Vol.7 No.12 December 2002
This is the first report of long-distance movement of AsA in plants and, given the proposed regulatory influence of AsA on cell division and growth implied by the phenotypes of various low AsA mutants, it has important implications for the regulation of sink development. Although there is some evidence for the existence of protein-based AsA transporters across plant cell plasma membranes, precisely how long-distance movement is effected remains to be determined. It is hoped that some insight might be gained from the functional analysis of 12 putative members of the nucleobase-ascorbate transporter family recently discovered in the
525
Arabidopsis genome. Because AsA is transported intact, this must now be a real goal for plant biotechnologists because the ability to manipulate AsA transport could provide an alternative strategy for increasing the amounts of AsA in sink tissues, many of which, such as potato tubers and fruits, are important food crops. 1 Franceschi, V. and Tarlyn, N. (2002) L-Ascorbic acid is accumulated in source leaf phloem and transported to sink tissues in plants. Plant Physiol. 130, 649–656
Nicola T. Wood [email protected]
A plant pathogen has a secret weapon When a fungal parasite infects a host plant, it can employ various strategies to suppress or evade host resistance mechanisms. Tomato plants, Lycopersicon esculentum, produce the glycosylated steroid α-tomatine, a saponin that has antifungal activity. The fungus that causes tomato leaf spot, Septoria lycopersici, secretes tomatinase, an extracellular enzyme that hydrolyses glucose from α-tomatine to give a product, β2-tomatine, that is substantially less toxic to the fungus, allowing it to colonize tomato plants. Now Kamal Bouarab and his colleagues [1] have found that tomatinase-deficient mutants of S. lycopersici trigger enhanced cell death and elevated expression of plant defense genes early in the infection process. This suggests that tomatinase interferes with the disease-resistance apparatus in tomato plants. To take advantage of virus-induced gene silencing (VIGS) methodology, Bouarab et al. switched to another solanaceous species, Nicotiana benthamiana, in which the S. lycopersici infection process also requires tomatinase. The fungus must secrete tomatinase to proliferate in leaf
tissue even though N. benthamiana does not produce α-tomatine. In the absence of tomatinase, the fungus triggers localized cell death. VIGS experiments were carried out to produce mutants of N. benthamiana in which the gene, SGT1, was silenced. The protein, SGT1, is a key component of the signal transduction pathways in plants that lead to disease resistance. ‘…tomatinase has another role in establishing disease besides the destruction of saponin-related phytoanticipins (antibiotics) in the host plant.’ The mutagenized plants were challenged with either the wild-type S. lycopersici strain or with the tomatinase-deficient mutant, 2D2. Whereas wild-type plants were resistant to the tomatinase-deficient mutant 2D2, the authors found that 2D2 caused extensive disease in leaves of SGT1-silenced plants, and, in the early stages of infection, was able to enter the stomata and grow around the mesophyll cells without triggering hypersensitive plant cell death. Thus, the hypersensitive-like response, observed when N. benthamiana leaves were challenged
with the tomatinase-deficient parasite, was dependent on SGT1 activity. The failure of tomatinase-deficient mutants to grow in wild-type N. benthamiana confirmed the authors’ view that tomatinase has another role in establishing disease besides the destruction of saponin-related phytoanticipins (antibiotics) in the host plant. It has usually been assumed that enzymes such as tomatinase are a pathogen’s virulence factors, which act by degrading the host’s protective antimicrobial secondary metabolites. It now appears that, in addition, the degradation products of tomatinase activity suppress host-resistance responses normally induced when the parasite colonizes its host, thereby providing another level of pathogen weaponry. It will be interesting to learn if other pathogens use similar mechanisms to suppress host resistance. 1 Bouarab, K. et al. (2002) A saponin-detoxifying enzyme mediates suppression of plant defences. Nature 418, 889–892
Richard C. Staples [email protected]
Dual role of plant mitochondria in promoting PCD or cell survival Programmed cell death (PCD) is a key event in plant development and stress responses, including the pathogen-induced hypersensitive response. As in animals and yeasts, plant PCD is often characterized by nuclear DNA fragmentation, a distinctive http://plants.trends.com
feature of necrotic cell death. The animal and yeast PCD, commonly termed apoptosis, is achieved by execution of mitochondria-dependent and -independent pathways. In the mitochondria-dependent pathway, mitochondria play a major
role in coordinating caspase activation through the release of cytochrome c in the cytosol; this release is tightly regulated by anti- and pro-apoptotic members of the Bcl-2 family of proteins. Therein, cytochrome c is rerouted from the
1360-1385/02/$ – see front matter © 2002 Elsevier Science Ltd. All rights reserved.
showed that AsA, rather than its metabolites, was transported. Endogenously produced AsA, monitored following the application of L-galactono-1,4-lactone (GAL-L) (the immediate precursor of AsA) to source leaves, was translocated in the same way. This was shown by a doubling of AsA levels in the shoot tip above the application leaf and no change in the mature leaves below it. GAL-L itself was not transported. Furthermore, because AsA levels in sinks increased in proportion to levels in the application leaf, sink tissue AsA content appears to be directly influenced by availability in source tissues.
TRENDS in Plant Science Vol.Vol.7 No.12 December 2002
This is the first report of long-distance movement of AsA in plants and, given the proposed regulatory influence of AsA on cell division and growth implied by the phenotypes of various low AsA mutants, it has important implications for the regulation of sink development. Although there is some evidence for the existence of protein-based AsA transporters across plant cell plasma membranes, precisely how long-distance movement is effected remains to be determined. It is hoped that some insight might be gained from the functional analysis of 12 putative members of the nucleobase-ascorbate transporter family recently discovered in the
525
Arabidopsis genome. Because AsA is transported intact, this must now be a real goal for plant biotechnologists because the ability to manipulate AsA transport could provide an alternative strategy for increasing the amounts of AsA in sink tissues, many of which, such as potato tubers and fruits, are important food crops. 1 Franceschi, V. and Tarlyn, N. (2002) L-Ascorbic acid is accumulated in source leaf phloem and transported to sink tissues in plants. Plant Physiol. 130, 649–656
Nicola T. Wood [email protected]
A plant pathogen has a secret weapon When a fungal parasite infects a host plant, it can employ various strategies to suppress or evade host resistance mechanisms. Tomato plants, Lycopersicon esculentum, produce the glycosylated steroid α-tomatine, a saponin that has antifungal activity. The fungus that causes tomato leaf spot, Septoria lycopersici, secretes tomatinase, an extracellular enzyme that hydrolyses glucose from α-tomatine to give a product, β2-tomatine, that is substantially less toxic to the fungus, allowing it to colonize tomato plants. Now Kamal Bouarab and his colleagues [1] have found that tomatinase-deficient mutants of S. lycopersici trigger enhanced cell death and elevated expression of plant defense genes early in the infection process. This suggests that tomatinase interferes with the disease-resistance apparatus in tomato plants. To take advantage of virus-induced gene silencing (VIGS) methodology, Bouarab et al. switched to another solanaceous species, Nicotiana benthamiana, in which the S. lycopersici infection process also requires tomatinase. The fungus must secrete tomatinase to proliferate in leaf
tissue even though N. benthamiana does not produce α-tomatine. In the absence of tomatinase, the fungus triggers localized cell death. VIGS experiments were carried out to produce mutants of N. benthamiana in which the gene, SGT1, was silenced. The protein, SGT1, is a key component of the signal transduction pathways in plants that lead to disease resistance. ‘…tomatinase has another role in establishing disease besides the destruction of saponin-related phytoanticipins (antibiotics) in the host plant.’ The mutagenized plants were challenged with either the wild-type S. lycopersici strain or with the tomatinase-deficient mutant, 2D2. Whereas wild-type plants were resistant to the tomatinase-deficient mutant 2D2, the authors found that 2D2 caused extensive disease in leaves of SGT1-silenced plants, and, in the early stages of infection, was able to enter the stomata and grow around the mesophyll cells without triggering hypersensitive plant cell death. Thus, the hypersensitive-like response, observed when N. benthamiana leaves were challenged
with the tomatinase-deficient parasite, was dependent on SGT1 activity. The failure of tomatinase-deficient mutants to grow in wild-type N. benthamiana confirmed the authors’ view that tomatinase has another role in establishing disease besides the destruction of saponin-related phytoanticipins (antibiotics) in the host plant. It has usually been assumed that enzymes such as tomatinase are a pathogen’s virulence factors, which act by degrading the host’s protective antimicrobial secondary metabolites. It now appears that, in addition, the degradation products of tomatinase activity suppress host-resistance responses normally induced when the parasite colonizes its host, thereby providing another level of pathogen weaponry. It will be interesting to learn if other pathogens use similar mechanisms to suppress host resistance. 1 Bouarab, K. et al. (2002) A saponin-detoxifying enzyme mediates suppression of plant defences. Nature 418, 889–892
Richard C. Staples [email protected]
Dual role of plant mitochondria in promoting PCD or cell survival Programmed cell death (PCD) is a key event in plant development and stress responses, including the pathogen-induced hypersensitive response. As in animals and yeasts, plant PCD is often characterized by nuclear DNA fragmentation, a distinctive http://plants.trends.com
feature of necrotic cell death. The animal and yeast PCD, commonly termed apoptosis, is achieved by execution of mitochondria-dependent and -independent pathways. In the mitochondria-dependent pathway, mitochondria play a major
role in coordinating caspase activation through the release of cytochrome c in the cytosol; this release is tightly regulated by anti- and pro-apoptotic members of the Bcl-2 family of proteins. Therein, cytochrome c is rerouted from the
1360-1385/02/$ – see front matter © 2002 Elsevier Science Ltd. All rights reserved.